Transcript Dermatoses Resulting from Physical Factors

Dermatoses Resulting from
Physical Factors
-Heat Injuries.
-Cold injuries.
-Solar injuries.
-Radiodermatitis.
-Presure indused diseases.
Heat Injuries
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Thermal Burns
Electrical Burns
Miliaria
Erythema Ab Igne
Thermal burns:
*First-degree burn:
There is active congestion of superficial blood vessels.
This causes erythema, sometimes followed by epidermal
desquamation.
Constitutional reactions occur if large area involved.
Pain and increased surface heat may be severe.
*Second-degree burn:
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Superficial
Transudation of serum
causing edema of
superficial tissues
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Deep
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Pale and anesthetic
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Vesicles and blebs
Complete recovery without
scar or blemish is usual
Injury to reticular dermis
compromises blood flow
and destroys appendages
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Healing takes > 1 month
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Scarring occurs
Second-Degree Burn
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Accidental scald
Splash-anddroplet pattern
of an accidental
scald from hot
cup of tea
*Third degree burn:
Full-thickness tissue loss.
Skin appendages are destroyed.
There is no epithelium for regeneration.
Healing leaves a scar.
*Fourth degree burn:
Destruction of entire skin and subcutaneous fat with any
underlying tendons
Electrical Burns:
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Contact- small but deep,
causing some necrosis of
underlying tissues
Flash-burns usually cover a
large area and are similar to
a surface burn and should
be tx as such
Lightning is the most lethal
type of strike, cardiac arrest
or other internal injuries
may occur
Electrical Burns
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Indirect- burns that are
either linear in areas at
which sweat was present;
are feathery or
aborescent pattern, which
is believed to be
pathognomonic
Miliaria
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Occlusion of eccrine sweat gland leads to retention of sweat with
failure of delivery of sweat to the skin surface.
Eventually backed-up pressure causes rupture of sweat gland or
duct at different levels.
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Escape of sweat into adjacent tissue produces miliaria.
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Common in hot, humid climates.
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Different forms of miliaria occur depending on the level of injury to
the sweat gland.
1. Miliaria crystalina:
-Small, clear, superficial vesicles without inflammation.
-Appears in bedridden pts and bundled children.
-Lesions are asymptomatic and rupture at the slightest
trauma.
-Self-limited; no treatment is required.
2. Miliaria rubra:
-Discrete, extremely pruritic, erythematous
papulovesicles with sensation of prickling, burning, or
tingling.
-Site of injury is prickle cell layer.
3. Miliaria pustulosa:
-Always preceded by some injury, destruction, or
blocking of sweat duct.
-Pustules are independent of hair follicle and sterile.
-Seen in intertriginous areas, flexure surfaces of
extremities, scrotum, and back of bedridden pts.
4. Miliaria profunda:
-Nonpruritic, flesh-colored, deep-seated, whitish papules
-Asymptomatic, usually lasting only 1 hr after
overheating has ended.
-Concentrated on the trunk and extremities.
-Occlusion is in the upper dermis.
-Only seen in tropics usually following a severe bout of
miliaria rubra.
Treatment:
-Mild cases may respond to dusting powders, such as
cornstarch or talcum powder.
-A lotion containing 1% menthol and glycerin and 4%
salicylic acid in 95% alcohol is effective.
-An oily “shake” lotion such as calamine lotion, with 1%
or 2% phenol may be effective.
Erythema (pigmentatio) Ab Igne
“toasted skin” syndrome:
-Persistent erythema or coarsely reticulated residual
pigmentation.
-Produced by long-continued exposure to excessive heat
without production of burn.
-It begins as a mottling caused by local hemostasis and
becomes a reticulated erythema, leaving pigmentation.
-No effective treatment; they may benefit from:
*Bland emollients.
*Kligman’s combination of 5% hydroquinone in
hydrophilic ointment containing 0.1% retinoic acid and
0.1% dexamethasone may reduce unsightly
Cold Injuries
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Chilblains
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Frostbite
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Immersion injury
Chilblains:
-Acute chilblains is the mildest form of cold injury,
characterized by inflamed purple-pink swellings on the
fingers, toes, and ears.
-There is pain, itching, or burning on rewarming, caused
by arteriolar and venular constriction.
-Patients are usually unaware of injury until they develop
burning, itching, and redness.
Treatment;
*Nifedipine 20mg TID, vasodilators (nicotinamide 100
mg TID or dipyridamole 25 mg TID),pentoxifylline may
be useful
*Smoking strongly discouraged
Frostbite:
Develops when soft tissue is frozen and locally deprived
of blood supply.
Frozen part is painless and becomes pale and waxy.
Four stages:
I- Frost-nip erythema, edema,cutaneous anesthesia &
transient pain.
II- second degree: hyperemia, edema & blistering, with
clear fluid in bullae.
III- third-degree: full-thickness dermal loss with
hemorrhagic bullae formation or waxy, dry, mummified
skin.
IV- Full-thickness loss of entire part.
Immersion Foot Syndromes
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Trench Foot
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Warm Water Immersion Foot
Trench Foot
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Term derived from trench
warfare in World War I, when
soldiers stood, sometimes for
hours, in trenches with a few
inches of cold water in them
Results from prolonged
exposure to cold, wet
conditions without immersion
or actual freezing
Tx-removal from environment
Dermatosis resulting from sun
exposure
Parts of solar spectrum important to photomedicine:
*Visible light 400 to 760 nm, has little biologic activity,
except for stimulating the retina
*Infrared radiation beyond 760 nm, experienced as
radiant heat.
*Below 400 nm is the ultraviolet spectrum, divided into
three bands:
-UVA, 320 to 400 nm
-UVB, 290 to 320 nm
-UVC, 200 to 290 nm
Virtually no UVC reaches the earth’s surface, because it
is absorbed by the ozone layer.
Skin Types
A.Sunburn and Solar Erythema:
-UVB is 1000 times more erythemogenic than UVA, so
most solar erythema is cause by UVB.
-UVA is 100 times greater than UVB radiation during the
midday hours.
-Sunlight early and late in the day contains more UVA.
-UVA is reflected from sand, snow, or ice to a greater
degree than UVB.
-Amount of ultraviolet exposure increases at higher
altitudes, is greater in tropical regions, and temperate
climates in summer.
Clinical signs and symptoms:
-Sunburn is normal cutaneous reaction to sunlight in excess of an
erythema dose (the amount that will induce reddening).
-UVB erythema peaks at 12 to 24 hrs after exposure.
-Desquamation is common about a week after sunburn even in
non-blistering areas.
Treatment:
-Cool compresses
-Topical steroids
-Topical remedy:
Indomethacin 100 mg
Absolute ethanol 57 ml
Propylene glycol 57 ml
spread widely over burned area with palms and let dry
Prophylaxis:
-Avoid sun exposure between 10 am and 2 pm.
-Barrier protection with hats and clothing.
-Sunscreen agents include UV-absorbing chemicals (chemical
sunscreens:, and UV-scattering or blocking agents (physical
sunscreens).
Sunscreens:
1. Chemical sunscreens: para-aminobenzoic acid (PABA), PABA
esters, cinnamates, salicylates, anthranilates, benzophenoes).
2. Physical agents: titanium/zinc dioxide.
3. Combinations of both.
*Water resistant: maintaining their SPF after 40 minutes of water
immersion.
*Water proof: maintaining their SPF after 80 mins of water
immersion.
*UVA protection: sunscreens containing benzophenones or
dibenzoylmethanes
*Apply sunscreen at least 20mins before sun exposure
B. Photoaging (Dermatohelioisis):
-Characteristic changes induced by chronic sun exposure
-Risk of developing these changes correlated with
baseline pigmentation (constitutive pigmentation) and
ability to resist burning and tan following sun exposure
(facultative pigmentation).
1. Poikiloderma of Civatte:
-Refers to reticulate hyperpigmentation with
telangiectasia, and slight atrophy of sides of the neck,
lower anterior neck and V of chest.
-Submental area is spared.
-Frequently presents in fair-skinned men and women in
their middle to late thirties or early forties.
2.Cutis rhomboidalis nuchae (sailor’s neck or
farmer’s neck):
-Characteristic of long-term, chronic sun exposure.
-Skin on back of neck becomes thickened, tough, and
leathery and normal skin marking become exaggerated.
Favre-Racouchot syndrome :
-Thickened yellow plaques studded with comedomes and
cystic lesions.
-Treatment is removal , retinoic acid cream, surgical
removal of cysts and redundant skin.
C. Photosensitivity:
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Photosensitizers may induce an abnormal reaction in skin
exposed to sunlight or its equivalent.
Substances may be delivered externally or internally.
Increased sunburn response without prior allergic sensitization
is called phototoxicity.
Phototoxicity may occur from both externally applied
(phytophotodermatitis and berloque dermatitis) or internally
administered chemicals (phototoxic drug reaction).
Phytophotosensitivity
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Plant-induced
photosensitivity-linear
hyperpigmentation on
the face following
exposure to limes and
sunlight.
Phytophotosensitivity
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Hyperpigmentation on
the dorsal aspect of
the hands following
the use of limes and
sunlight exposure.
Phototoxic Drug Reactions:
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Most occur from tetracyclines, nonsteroidal antiinflammatory
drugs, amiodarone, and phenothiazines.
Action spectrum for all is in the UVA range.
In the case of amiodarone and chlorpromazine,
hyperpigmentation is a well-recognized pattern of phototoxicity.
It causes slate blue (amiodarone) or slate gray
(chlorpromazine) coloration, resulting from drug deposition in
the tissues.
Amiodarone
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Phototoxic reaction to
a nonsteroidal
antiinflammatory drug
Phototoxicity vs photoallergy:
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In the case of external contactants –
phototoxicity occurs on initial exposure, has
onset < 48 hrs, occurs in most people exposed
to the phototoxic substance and sunlight.
Photoallergy, in contrast, occurs only in
sensitized persons, may have delayed onset, up
to 14 days (a period of sensitization), and shows
histologic features of contact dermatitis.
Photosensitivity
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Drug-induced
photosensivityphotoallergic
dermatitis on sunexposed areas of
an infant following
topical use of
hexachlorophene.
Photoallergic dermatitis
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Papulovesicular
lesions of
photoallergic
dermatitis due to
hexachlorophene.
Drug induced photosensitivity
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The erythema is less
apparent in black
skin, but the
involvement of the
nose in this patient
suggests
phototoxicity, in this
case caused by
thiazide
Drug induced photosensitivity
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The backs of the
hands are the classic
sites to be involved in
light induced eruption
Idiopathic photosensitivity:
1. Polymorphous Light Eruption
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Most common form of sensitivity.
All races and skin types affected.
Typically in first three decades.
Females outnumber males.
Unknown pathogenesis.
Positive family history in 10-50% of pts.
Different morphologies seen, although in the
individual the morphology is constant.
PMLE
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Exposed areas such
as the backs of the
hands and forearms
are affected.
Ultraviolet A is
mainly responsible
and may penetrate
window glass.
PMLE
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The patchiness of the edematous papules and
plaques is characteristic.
PMLE
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The eruption is less red and confluent than a
sunburn (left).
Lesions are typically papular & clustered (right).
2. Actinic Prurigo
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The clinical features
are somewhat
suggestive of PML,
but the lesions are
persistent, mostly in
children with crusted
papules, and the HLA
type was DR4 (occurs
in 80-90% of AP pts).
AP
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Severe actinic prurigo shows spread to buttocks (left)
Arms show crusted papules that are denser distally;
they are also worse in summer
3. Hydroa Vacciniforme
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Photodermatosis with onset in childhood.
Lesions appear in crops with disease free intervals.
Attacks may be preceded by fever and malaise.
Ears, nose, cheeks, and extensor arms and hands are
affected.
Within 6 hrs of exposure stinging may occur.
There is an early, PML-like eruption, but with vesicles
around the mouth and umbilicated lesions on the nose.
A later, more severe example shows vesiculation with
umbilication, but also marked hemorrhagic crusting.
Hydroa Vacciniforme
Hydroa Vacciniforme
Radiodermatitis:
Acute Radiodermatitis:
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With an “erythema dose” of ionizing radiation
there is a latent period of up to 24 hrs before
visible erythema develops.
Initial erythema lasts 2-3 days but may be
followed by a second phase beginning up to 1
week after the exposure and lasting up to 1
month.
Acute Radiodermatitis
(fluoroscopic induced)
Chronic Radiodermatitis:
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Chronic exposure to “sub erythema” doses of ionizing
radiation over a prolonged period will produce varying
amounts of damage to skin and underlying tissues after a
variable latent period of several months to several decades.
Telangiectasia, atrophy, and hypopigmentation with residual
focal increased pigment (freckling) may appear.
Radiation Cancer:
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After a latent period averaging 20 –30 yrs,
various malignancies may develop
Most frequent are basal cell carcinomas
Next frequent are squamous cell carcinomas
These may occur in sites of prior radiation even
without evidence of chronic radiation damage
SCCs arising in sites of radiation therapy
metastasize more frequently than purely suninduced SCCs
Other cancers induced by radiation:
angiosarcoma, malignant fibrous histiocytoma,
sarcomas, and thyroid carcinoma
Radiation Cancer
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SCC developing in a
chronic radiation ulcer
on the chest
Callus:
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Nonpenetrating, circumscribed hyperkeratosis
produced by pressure.
Occurs on parts subject to intermittent pressure
(palms, soles, bony prominences of the joints).
Callus differs from clavus (corn) in that a callus has no
penetrating central core and is a more diffuse
thickening.
Calluses tend to disappear spontaneously when
pressure is removed.
Dermatosis resulting from presure:
1. Clavus (Corns):
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Circumscribed, horny, conical thickenings with the
base on the surface and the apex pointing inward and
pressing on adjacent structures.
Two types: hard and soft.
Hard: occur on dorsa of toes or on soles.
Soft: occur between toes, softened by macerating
action of sweat.
Plantar corns can be differentiated from plantar
warts by paring off the surface keratin until either
the pathognomonic elongated dermal papillae of
the wart with its blood vessels, or the clear horny
core of the corn can be visualized.
2. Pressure Ulcers (Decubitus):
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The bedsore is a pressure ulcer produced anywhere
on the body by prolonged pressure.
Caused by ischemia of underlying structures of skin,
fat, and muscles resulting from sustained and
constant pressure.
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Usually in chronically debilitated persons unable to
change position.
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Bony prominences of body are most frequently
involved.
Care and treatment:
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Clean wounds initially and at each dressing change via
nontraumatic technique.
Normal saline is best.
Dressing selection should maintain moist environment.
Occlusive dressings like film and hydrocolloid are often
utilized.
Surgical debridement with reconstructive procedures may
be needed (except stable heel ulcers (do not need
debridement if only a dry eschar is present).
Electrical stimulation of refractory ulcers may be beneficial.
3. Friction Blisters:
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Formation of vesicles or bullae occurring at sites of
combined pressure and friction.
Enhanced by heat and moisture.
Examples: feet of military recruits in training, palms of
oarsmen not having developed protective calluses,
beginning drummers (“drummer’s digits”).
4. Black Heel:
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-Also called talon noir or
calcaneal petechiae.
-A sudden shower of minute
macules occurs most often
on the posterior edge of the
plantar surface of one or
both heels.
-Sometimes occurs distally
on one or more toes.
-Black heel is seen in
basketball, volleyball, tennis,
or lacrosse players
5. Painful Fat Herniation:
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Painful piezogenic pedal papules.
Rare cause of painful feet representing fat herniations through
thin fascial layers of weight-bearing parts of the heel.
These dermatoceles become apparent when wt is placed on the
heel.
These disappear when pressure is removed.
Extrusion of fat tissue together with its blood vessels and
nerves initiates pain on prolonged standing.
Avoidance of prolonged standing is the only way to provide
relief.
Majority of people experience no symptoms.
Narcotic Dermopathy:
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Heroin(diacetylmorphine) is a narcotic prepared by dissolving
the heroin powder in boiling water and then injecting it.
Favored route is IV.
Resulting in thrombosed, cordlike, thickened veins.
Narcotic Dermopathy
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Subcutaeous injection (“skin popping”) can
result in multiple, scattered ulcerations, which
heal with discrete atrophic scars